Exam 4 - Endocrine Flashcards
1
Q
Liver is the primary sournce of endogenous glucose production via what 2 processes?
A
glycogenolysis & gluconeogenesis
s2
2
Q
what are the Hyperglycemia-producing hormones and why are they important?
A
- glucagon, epinephrine, growth hormone, and cortisol
- they comprise the glucose counterregulatory system and support glucose production
s3
3
Q
What is the common s/e of metformin? Who is it contraindicated for?
A
GI side effects.
Contrainidicated with renal insufficiency.
S10
4
Q
what are some facts regarding etiology of Type 2 DM?
A
- Accounts for >90% DM cases
- Increasingly seen in younger pts & children over the past decade
- Very underrecognized, normally present 4-7 years before diagnosed
s6
5
Q
What is the initial tx for DMII?
A
Lifystyle changes and Metformin
S10
6
Q
What are the additional therapies for DMII?
A
Insulin
Sulfonylurea
GLP-1 receptor agonist
Thiazolidenedione
glinide
SGLT-2 inhibitor
DPP-4 inhibitor
a- glucosidase inhibitor
Pramlintide
S10
7
Q
Insulin is necessary in ____ DMI cases & ____ DMII cases
A
all
30%
S11
8
Q
Types of insulin
A
- Rapid acting (Lispro, Aspart)
- Short acting (regular)
- Basal/intermediate acting (NPH, Lente)
- Long acting (Ultralente, Glargine)
S11
9
Q
What is the most dangerous complication of insulin? What is it exacerbated by?
A
Hypoglycemia.
Exacerbated by ETOH, metformin, sulfonylureas, ACE-I’s, MAOI’s, Non-selective BB’s
S11
10
Q
What does repetitive hypoglycemic episodes can lead to? What is the tx for hypoglycemia?
A
“Hypoglycemia unawareness”
Pt becomes desensitized to hypoglycemia and doesn’t show autonomic sx.
Neuroglycopenia ensues→fatigue, confusion, h/a, seizures, coma.
Tx: PO or IV glucose (may give SQ or IM if unconscious)
S11
11
Q
What is the onset/peak/duration of short acting insulin (Human Regular, Lispro, Aspart)?
A
S12
12
Q
What is the onset/peak/duration of intermediate insulin (Human NPH, Lente)?
A
S12
13
Q
What is the onset/peak/duration of long acting insulin (ultralente, glargine)?
A
S12
14
Q
Plasma insulin levels (chart)
Memorize
A
S12
15
Q
What are the diagnostic features of DKA?
A
S13
16
Q
What is a complication of decompensated DM? what its mortality rate?
A
Diabetic Ketoacidosis
mortality 1-2%
S13
17
Q
DKA is more common in which type of DM? What can trigger DKA?
A
DKA more common in DMI, often triggered by infection/illness
S13
18
Q
How does high glucose affect the renal function?
A
High glucose exceeds the threshold for renal reabsorption creating osmotic diuresis & hypovolemia.
S13
19
Q
What causes the overproduction of ketoacids?
A
Tight metabolic coupling of gluconeogenesis & ketogenesis.
DKA results in excessive glucose-counterregulatory hormones, with glucagon activating lipolysis & free fatty acids→ substrates for ketogenesis.
S13
20
Q
What is the treatment for DKA?
A
- IV volume replacement
- Insulin: Loading dose 0.1u/kg Regular + low dose infusion @ 0.1u/kg/hr
- Correct acidosis: sodium bicarb
- Electrolyte supplement: k+, phos, mag, sodium
*Correction of glucose w/o simultaneous correction of sodium may result in cerebral edema
S14
21
Q
What are the characteristics of hyperglycemic hyperosmolar syndrome? What is the mortality rate of HHM?
A
severe hyperglycemia, hyperosmolarity & dehydration
Mortality 10-20%
S15
22
Q
What are the signs and symptoms of Hyperglycemic Hyperosmolar Syndrome?
A
- Polyuria
- polydipsia
- hypovolemia
- HoTN
- tachycardia
- organ hypoperfusion
- Some degree of acidosis, but not DKA
Hyperosmolarity leads to coma.**
S15
23
Q
What is the treatment of Hyperglycemic Hyperosmolar Syndrome?
A
fluid resuscitation, insulin bolus + infusion, e-lytes
S15
24
Q
What happens when glucose load exceeds renal glucose absorption?
A
Mass solute diuresis
S15
25
What is the microvascular complication of DM?
Nonocclusive microcirculatory dz w/impaired blood flow autoregulation
## Footnote
S16
26
What is the neuropathic complication of DM associated w/ renal fx?
30-40% DM1, 5-10% DM2 develop **ESRD**. Kidneys develop glomerulosclerosis, arteriosclerosis, & tubulointerstitial disease
## Footnote
S16
27
What are the signs of DM related ESRD?
HTN, proteinuria, peripheral edema,↓GFR
## Footnote
S16
28
What causes hyperkalemia in patients with ESRD?
When GFR < 15-20, kidneys no longer clear K+, Pts become hyperkalemic & acidotic
## Footnote
S16
29
What is the treatment for ESRD?
* ESRD tx: HD, PD, kidney transplant
* **ACE-I’s** slow progression of proteinuria and the rate of GFR slowing
Combined kidney-pancreas transplant may prevent recurrent nephropathy
## Footnote
S16
30
What is characteristic of DM peripheral neurophathy? How does it progress?
Normally a **distal symmetric** diffuse sensorimotor polyneuropathy.
Starts in toes/feet, progresses **proximally**
## Footnote
S17
31
Loss of which fibers cause the reduction in light touch and proprioception?
large sensory & motor fibers
## Footnote
S17
32
Loss of which fibers cause the decrease in pain/temperature perception leading to neuropathic pain?
Small nerve fibers
## Footnote
S17
33
What causes the significant morbidity in someone w/ peripheral neuropathy?
Recurrent infections & amputation wounds.
## Footnote
S17
34
What medication doesn’t affect the underlying abnormality, but may relieve sx of Graves disease?
Beta Blockers
Propranolol impairs the peripheral conversion of T4 to T3
## Footnote
S28
35
What is the treatment of peripheral neuropathy?
optimal glucose control, NSAIDS, antidepressants, anticonvulsants
## Footnote
S17
36
What is diabetes related retinopathy?
* microvascular changes including vessel occlusion, dilation, ↑permeability, microaneurysms
* Visual impairment ranges from color loss to blindness
## Footnote
S17
37
What is a
General
Psych
s/s of Hyperparathyroidism?
General: **Anxious**
Psych: **Emotionally unstable**
## Footnote
S26 table
38
# DM complications
What causes autonomic neuropathy?
## Footnote
damaged vasoconstrictor fibers, impaired baroreceptors and ineffective CV activity!
## Footnote
18
39
What are the CV and GI s/s of autonomic neuropathy?
What is the treatment?
CV: abnormal HR control (variability), vascular dynamics, resting tachycardia, orthostatic hypotension and dysrhythmias
GI: N/V, bloating, impaired secretions & mobility--> gastroparesis
Tx: glucose control, small meals, prokinetics
## Footnote
18
40
What do you emphasize in patients with DM in the preop eval?
-emphasize CV, renal, neurologic, & muscoskeletal systems
-silent ischemia is possible!
-meticulus attention to hydration, preserve RBF!
-Consider stress test if multiple cardiac risk factors and poor exercise tolerance
## Footnote
19
41
What are diabetics at risk for in regards to anesthesia?
-Arrhythmia risk d/t autonomic neuropathy
-risk for aspirations d/t gastroparesis
* hold PO hypoglycemic and noninsulin injectables
## Footnote
19
42
Who is at risk for insulinoma?
Dx is based on whipple triad..what are they?
## Footnote
Insulinoma- benign insulin secreted pancreatic islet tumor
-occurs 2x in women than men~ 50-60 y/o
-Whipple triad:
hypoglycemia w fasting, glucose <50 w symptoms, and symptom release w glucose
-
## Footnote
20
43
Insulinoma pt's have high insulin levels during 48-72 hr fast (dx). What meds should you give them preop?
diaxoide, inhibits insulin release from B cells
-verapamil, phenytoin, promanalol, glucorticoids and ocreotide
-they’re at risk for hypoglycemia intraop** then hyperglycemia when tumor is removed
## Footnote
20
44
# Thyroid gland is composed of 2 lobes joined by an isthmus.
Where is the thyroid gland located?
What is located on the posterior aspect of each lobe?
-The gland is affixed to the anterior & lateral trachea, with upper border just below the cricoid cartilage
-parathyroid gland located on posterior aspect of each lobe
## Footnote
21
45
What innervates the rich capillary network in the thyroid gland?
What nerves are close to it?
Adrenergic and cholinergic systems innervate capillary network.
-recurrent laryngeal nerve and external motor branch of superior laryngeal nerve
## Footnote
21
46
Thermal thyroid scans evaluate thyroid nodules as warm if they are ____ functioning, hot if they are ____ and cold if they are ____
normally, hyperfunctioning and hypofunctioning
## Footnote
24
47
What can reduce the progression of retinopathy?
Glycemic control & BP control
## Footnote
S17
48
What does a decrease in TSH cause?
What does an increase in TSH cause?
-decreased T3 & T4 synthesis, decreased follicular cell size, and decreased vascularity
-increase in TSH yields an increase in hormone production, gland cellularity and vascularity
## Footnote
23
49
What type of cells does the thyroid gland contain?
What is thyroglobulin?
parafollicular cells- which produce calcitonin
-thyroid is composed of follicles filled w/ thyroiglobulin, which is an iodinated glycoprotein and substrate for thyroid hormone synthesis
## Footnote
21
50
What 3 glands regulate thyroid function?
hypothalamus, pituitary, and thyroid glands, in a classic feedback control system
## Footnote
23
51
What are top 3 pathologies for hyperthyroidism?
Graves disease
toxic multinodular goiter
toxic adenoma
## Footnote
25
52
What is the best test of thyroid hormone action at cellular level?
What is normal TSH level
TSH assay
normal TSH level is 0.4-5.0 milliunits/L
## Footnote
24
53
s/s of hyperthyroidism?
T3 acts directly on what?
hypermetabolic state: sweating, heat intolerance & fatigue w/inability to sleep, osteoporosis and weight loss
T3 acts directly on the myocardium and peripheral vasculature to cause cardiovascular responses
## Footnote
25
54
We eat iodide, it is reduced in the GI tract and absorbed, then transported to follicular cells. Iodide then binds to thyroglobulin with the help of what enzyme?
After that, how do we form active T3, T4?
binding of iodide to thyroglobulin is catalyzed by an iodinase enzyme and yields inactive monoiodotyrosine and diiodotyrosine.
Then, T1 and T2 undergo coupling w/ thyroid peroxidase to form T3 and T4
## Footnote
22
55
In the blood, what 3 proteins do T4 and T3 reversibly bind to?
What’s T4/T3 ratio?
thyroxine-binding globulin (80%), prealbumin (10–15%), and albumin (5–10%).
10:1
## Footnote
22
56
What are HEENT s/s of Hyperthyroidism?
* Flushed face
* Fine hair
* Exophthalmos/proptosis
## Footnote
S26 table
57
What are
CV
GI
Skin
s/s of Hyperthyroidism?
CV: **Palpitation**
GI: **Frequent BM/ Diarrhea**
Skin: **Warm, moist**
## Footnote
S26 table
58
What are Neurogical s/s of Hyperthyroidism?
* Wasting, weakness, fatigue of proximal limb muscles
* fine tremor of hands
* hyperactive DTR (deep tendon reflexes)
## Footnote
S26 table
59
What are Cardiac effects of Hyperthyroidism?
* Tachycardia, arrythmias (atrial)
* Hyperdynamic
* ↑ C.O. and contractility
* Cardiomegaly
## Footnote
S26 table
60
What is the diagnosis that confirms Graves disease?
**TSH antibodies** in the context of
**↓ TSH and ↑ T3 & T4**
## Footnote
S27
61
What can enlarged goiter cause with Graves Disease?
* dysphagia
* globus sensation
* inspiratory stridor (from tracheal compression)
## Footnote
S27
62
What are s/s of Graves disease?
* diffusely enlarged thyroid
* Ophthalmopathy (in 30% cases)
* enlarged goiter
## Footnote
S27
63
Grave disease is ____, caused by thyroid-stimulating ____ that bind to ____ receptors, stimulating growth, vascularity, and hypersecretion
Grave disease is **autoimmune**, caused by thyroid-stimulating **antibodies** that bind to **TSH** receptors, stimulating growth, vascularity, and hypersecretion
## Footnote
S27
64
What is the leading cause of hyperthyroidism, effecting 0.4% population?
Who does this typically occurs in?
**Graves disease**
Typically occurs in
**females** (7:1 in 20-40 y/o)
## Footnote
S27
65
What is the 1st line treatment of Graves disease?
**Antithyroid drug**
Either Methimazole or Propylthiouracil (PTU)
## Footnote
S28
66
What treatment is recommended when medical treatments failed with Graves disease?
Ablative therapy or surgery
**subtotal thyroidectomy** > has lower incidence of hypothyroidism than radioactive iodine therapy
## Footnote
S28
67
What are complications from surgery for Graves disease?
* hypothyroidism
* hemorrhage with tracheal compression
* RLN (recurrent laryngeal nerve) damage
* damage to parathyroid glands
## Footnote
S28
68
What treatment for Graves disease is reserved for pre-op or thyroid storm and why?
high concentrations of iodine (this inhibits TH release)
The effect is short lived
## Footnote
S28
69
Pre-op considerations for Graves disease are:
____ ____ should be established pre op
Elective cases may need to wait ____ weeks for antithyroid drugs to take effect
**Thyroid levels** should be established pre op
Elective cases may need to wait **6-8** weeks for antithyroid drugs to take effect
## Footnote
S29
70
What drugs are usually necessary in emergent cases of Graves disease?
* IV Beta-Blockers
* Glucocorticoids
* PTU
## Footnote
S29
71
Why do you need to evaluate upper airway of pt with Graves Disease pre-operatively?
for evidence of **tracheal compression or deviation** caused by a goiter
## Footnote
S29
72
What is a life-threatening exacerbation of hyperthyroidism precipitated by trauma, infection, medical illness, or surgery?
What is the mortality rate?
Thyroid Storm
20% mortality rate
## Footnote
S30
73
What kind of condition presents very similar to Thyroid storm and differentiation between the two can be extremely difficult?
Malignant Hyperthermia
## Footnote
S30
74
____ levels in thyroid storm may not be much higher than basic hyperthyroidism
Thyroid hormone
## Footnote
S30
75
When do Thyroid storm most often occurs?
**postoperatively** in *untreated or inadequately treated* hyperthyroid pts
## Footnote
S30
76
What are the treatments for Thyroid storm?
* rapid alleviation of thyrotoxicosis
* supportive care
## Footnote
S30
77
What is another name for Hypothyroidism?
What is the course of this disease in adults?
Myxedema
a slow, progressive course
## Footnote
S31
78
What are the lab results of primary Hypothyroidism?
↓ T3 & T4 production with adequate TSH
## Footnote
S31
79
What is the 1st common cause of Hypothyrodism?
What is the 2nd common cause?
1st common cause: **ablation of the gland**
(by radioactive iodine or sx)
2nd common cause: **idiopathic and probably autoimmune**
(antibodies blocking TSH receptors)
## Footnote
S31
80
What is an *autoimmune disorder *characterized by goitrous enlargement and hypothyroidism that usually affects middle-aged women?
Hashimoto thyroiditis
## Footnote
S31
81
What other syndrome commonly occurs with Hypothyroidism?
SIADH
## Footnote
S31
82
What are the general and psych symptoms of Hypothyroidism?
General symptoms:
-fatigue
-listlessness
-weight gain
Psych:
apathy
## Footnote
S31 and S32 table
83
What are the HEENT symptoms of Hypothyroidism?
* dry brittle hair
* large tongue
* deep hoarse voice
* periorbital edema
## Footnote
S31 and S32 table
84
What are the neurologic symptoms of Hypothyroidism?
* slow speech
* slowing of motor function
* prolonged relaxation phase of DTR
## Footnote
S31 and S32 table
85
What are the GI symptoms of Hypothyroidism?
* constipation
* slow GI function
* adynamic ileus may occur
## Footnote
S31 and S32 table
86
What are the skin symptoms of Hypothyroidism?
* pale
* cool
* dry
* thickened
* non-pitting peripheral edema
* cold intolerance
## Footnote
S31 and S32 table
87
what is the most common endocrine disease and how common is it?
Diabetes Mellitus
affects 1 in 10 adults
## Footnote
s4
88
What are the respiratory symptoms of Hypothyroidism?
* fluid overload
* pleural effusions
* dyspnea
## Footnote
S31
89
What are the cardiac effects of Hypothyroidism?
* ↓ C.O.
* Baroreceptor function impaired
* Hypothyroid cardiomyopathy
* Pericardial effusions
on EKG:
* Flattened or inverted T waves
* low-amplitude P waves & QRS complexes
* Sinus bradycardia
* Ventricular dysrhtymias
## Footnote
S31 and S32 table
90
Myxedema Coma is triggered by what type of pathologies?
* infection
* trauma
* cold
* CNS depressants
## Footnote
Slide 35
91
What is a rare form of hypothyroidism characterized by delirium, hypoventilation, hypothermia, bradycardia, HoTN, and severe dilutional hyponatremia?
## Footnote
Slide 35
Mxyedema
Coma
## Footnote
35
92
what is glucagon's primary role?
stimulating glycogenolysis & gluconeogenesis, and inhibiting glycolysis
## Footnote
s3
93
what precedes onset of symptoms in type 1 DM?
long pre-clinical period (9-13 yrs) of B-cell antigen production
## Footnote
s5
94
Hypothermia is a ____feature that determine impaired thermoregulation
cardinal
## Footnote
Slide 35
95
Myxedema Coma occurs most commly in what population of patients
elderly women with a long history hypothyroidism?
## Footnote
Slide 35
96
Myexdema Coma is a medical emergency, What is the mortality percentage?
> 50%
## Footnote
Slide 35
97
What leads to diabetes mellitus?
and what does DM lead to w/ glucose?
an inadequate supply of insulin and/or an inadequate tissue response to insulin
* DM leads to increased circulating glucose levels with eventual microvascular and macrovascular complications
## Footnote
s4
98
What are treatments plan for Myxedema Coma
| *long list*
* IV L-thyroxine
* IV L- triiodothyroine
* IV - hydration with glucose- saline solutions
* Tempature regulation
* Correction of electrolytes implance
* Stabliization of cardiac and pulmonary system
## Footnote
Slide 35
99
True or false: Mechanical ventilation is not frequently required
false, mechanical ventilation is frequently required
## Footnote
Slide 35
100
what is type 1A DM caused by?
T-cell–mediated autoimmune destruction of β cells within pancreatic islets resulting in minimal or absent circulating levels of insulin
## Footnote
s4
101
what is type 1B DM?
rare disease of absolute insulin deficiency that is not immune mediated
## Footnote
s4
102
what happens in the initial stages of type 2 DM regarding insulin?
insensitivity to insulin on peripheral tissues leads to ↑pancreatic insulin secretion
## Footnote
s6
103
what is type 2 DM? is it immune mediated?
DM type 2 is not immune mediated
and results from defects in insulin receptors and post-receptor intracellular signaling pathways
## Footnote
s4
104
what are the key facts for type 1 DM regarding etiology?
is type 1 cause known?
* Accounts for 5-10% of all DM cases
* Usually diagnosed before age 40
Exact autoimmune cause of type 1a is **unknown**
## Footnote
s5
105
What are the 3 vitial signs that improve within 24 hours of given electrolyte ?
* Heart Rate
* BP
* Temp
## Footnote
Slide 35
106
Swelling of thyroid gland determine by hypertrophy & hyperplasia of follicular epithelium can be define as a......
Goiter & Thyroid Tumors
## Footnote
Slide 36
107
What are the causes of Goiter & Thyroid Tumors?
* lack of iodine
* ingestion of goitrogen (cassava,phenylbutazone, lithium)
* defect in the hormonal biosynthetic pathway
## Footnote
Slide 36
108
Goiter and Thyroid Tumors are assoicated with what type of compenstated state?
Euthyroid
## Footnote
Slide 36
109
Goiter and Thyriod Tumors are treated with what type of medication in most cases?
L-thyroxine
## Footnote
Slide 36
110
When is surgery indicated for a Goiter and thyroid Tumors?
* medical therapy is ineffective
* compromises of air way
* cosmetically unacceptable
## Footnote
Slide 36
111
What pathology during pre-op history would be predictive of possible airway obstruction during general anesthesia?
dyspnea in upright or supine postition
## Footnote
Slide 37
112
what is hyperglycemia over several days/weeks associated with in type 1 DM?
fatigue, weight loss, **polyuria**, polydipsia, blurry vision, hypovolemia, ketoacidosis
- she mentioned POLYURIA loudly lol
## Footnote
s5
113
how much of b cell function is lost before hyperglycemia even shows up in type 1 DM?
At least 80-90%
## Footnote
s5
114
What imaging testing is used to examine and assess the extent of the tumor?
CT
## Footnote
Slide 37
115
Which pulmoary funtion test is used to demonstrate the site and degree of obstruction?
The test is given with the patient in what 2 positions?
* FLow - volume loop
* upright and supine postition
## Footnote
Slide 37
116
as type 2 DM progresses, what happens to pancreas and insulin levels?
pancreatic function decreases & insulin levels become inadequate
## Footnote
s6
117
what are the 3 main abnormalities in DM2?
* ↑hepatic glucose release caused by a reduction in insulin’s inhibitory effect on liver
* Impaired insulin secretion
* Insufficient glucose uptake in peripheral tissues
## Footnote
s6
118
____ in the inspiratory limb of the loop indicate ____-thoracic obstruction
____ flow in the expiratory limb indicates an ____-thoracic obstruction
* Limitations, extra-thoracic obstructions
* Delayed, intra-thoracic obstructions
## Footnote
Slide 37
119
what's 2 tests are used for the diagnosis for DM2?
fasting blood glucose and HbA1c
## Footnote
s7
120
what is DM2 characterized by?
insulin resistance in skeletal muscle, adipose & liver
## Footnote
s7
121
what are the 3 causes of insulin resistance?
what may also contribute regarding lifestlye?
* Abnormal insulin molecules
* Circulating insulin antagonists
* Insulin receptor defects
OBESITY AND SEDENTARY LIFESTYLE also contribute!
## Footnote
s7
122
What type of imaging test can be adminstered to a patient who has a goiter or thyroid tumor in an upright and/or supine position to indicate the degree of cardiac compression ?
Echocardiogram
## Footnote
Slide 37
123
what HbA1c is considered normal?
prediabetic?
diabetic?
normal: <5.7%
prediabetic: 5.7-6.4%
diabetic: **>/=** 6.5%
## Footnote
s8
124
what is the american diabetes assoc criteria for dx of diabetes?
1. A1c >/= 6.5
2. Fasting Plasma Glucose >/= 126 mg/dL (7.0 mmol/L)* and fasting for at least 8 hrs!*
3. 2-hr plasma gluc >/= 200 mg/dL during glucose tolerance test
4. *in pt with classic symptoms of hyperglycemia or hyperglycemia crisis a random plasma gluc of >/= 200 mg/dL
## Footnote
s8
125
What is the morbidity percentage regarding thyroid surgery?
13%
## Footnote
Slide 38
126
what is the DM2 treatment? (3 things)
* Dietary adjustments
* Exercise/weight loss
* PO antidiabetic drugs - metformin (preferred initial med tx) and/or sulfonylureas
## Footnote
s9
127
Right laryngeal nerve injury can be____ or bilateral and temporary or ____.
* unilateral
* permanent
## Footnote
38
128
what drug class is metformin? and how does it help DM2?
A biguanide - preferred initial drug tx
* Enhances glucose transport into tissues
* ↓TGL & LDL levels
## Footnote
s9
129
what do sulfonylureas do?
what are some side effects?
* stimulate insulin secretion
* Enhances glucose transport into tissues
SE’s include hypoglycemia, weight gain & cardiac effects
## Footnote
s9
130
why are sulfonylureas not effective long term?
* d/t diabetic progressive loss of B cell function
## Footnote
s9
131
Parathyroid dysfx ::
* The ___ parathyroid glands are behind upper & lower poles of the thyroid gland + produce _______, which is released into the circulation by a _________ feedback that depends on plasma _______ level
* __________ stimulates the release of PTH
* ___________ suppresses hormonal synthesis and release
* PTH maintains normal plasma calcium level by promoting the movement of calcium across ________, __________, and ________.
4 ... parathyroid hormone (PTH) ... negative ... calcium
Hypocalcemia
hypercalcemia
GI tract, renal tubules, and bone
## Footnote
53
132
Hyperparathryoidism ::
* Present when secretion of PTH is ________
* Serum calcium concentrations may be _______, ______, or ______
* Hyperparathyroidism is classified as _____, ______, or _______
increased
increased, decreased, or unchanged
primary, secondary, or ectopic
## Footnote
54
133
ACTH- Independent Cushing: _____ cortisol production by abnormal _________ tissue that is not regulated by ____ and ACTH.
* excessive
* adrenocortical
* CRH
| 44
134
Acute Ectropic ACTH syndrome is a form of ACTH -_______ Cushing that is the most often associated with _______ __________ __________ carcinoma.
* dependent
* Small Cell Lung
| 44
135
In ACTH- Independent Cushing:
* CRH and ACTH levels are _________
* ______ or ______ ______ tumors are the most common cause of ACTH-independent Curshing Syndrome.
* suppressed
* Benign or Malignant Adrenocortical
| 44
136
Secondary Hyperparathyroidism ::
__________ response of the parathyroid glands to counteract a separate disease process producing _________ s/a CRF
o adaptive, it seldom produces ____________
o Tx ?? (2)
compensatory ... hypocalcemia
hypercalcemia
treat underlying cause
phosphate binder - renal pts to normalize serum phos
## Footnote
55
137
Symptoms of Hypercortisolism (Cushing Syndrome) are:
* Sudden weight ____.
* ↑_______ fat (______ face)
* Ecchymoses
* HTN
* ______________ intolerance
* muscle __________
* depression
* insomnia
* weight gain
* facial
* Moon
* intolereance
* wasting
| 45
138
Hypoparathyroidism ::
* Present when PTH is_________ or peripheral tissues are_________ to its effects
* Absence or deficient PTH is almost always__________, reflecting inadvertent removal of parathyroid glands, as during _____
* Pseudohypoparathyroidism is a________ disorder where PTH is adequate, but the ________ are unable to respond to it
deficient ... resistant
iatrogenic ... thyroidectomy
congenital ... kidneys
## Footnote
56
139
Diagnosis of Hypercortisolism (Cushing Syndome is done with ___ hour urine ______.
* 24 hour urine cortisol
| 45
140
Distinguishing Cushings ACTH Dependent from ACTH Independent involves measuring ________ ACTH and ________________ assays.
* plasma
* immunoradiometric
| 45
141
A high-doses dexamethasone suppression test distringuishes _______ from ______ ACTH Syndrome.
* Cushing's
* Ectopic
| 45
142
In Hypercortisolism (Cushing Syndrome) Imaging is useful for determining tumor ______________, but isn't helpfu if gauging _________ function.
* location
* adrenal
| 45
143
Treatment of choice for Hypercortisolism (Cushing Syndrome):
* transsphrenoidal _______________ if ________ is resectable.
* Alternatively, 85-90% resection of the _______ pituitary.
* microadrenomectomy
* microadenoma
* anterior pituitary
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144
Hypercortisolism (Cushing Syndrome): Surgical adrenolectomy is the treatmetn for adrenal __________ or ___________.
* adenoma
* carcinoma
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145
Pituitary ________ and bilateral total ___________ are necessary for some patients with Cushings.
* irradation
* adrenalectomy
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146
Pre-Op Considerations for Cushing Syndome:
* evaluate/treat ____,
* ______ balance
* blood glucose
* Consider ____________ in position
* BP
* Electrolye
* Osteoporosis
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147
Name the (8) Classic Signs of Cushings Syndome:
* Fat Pad: _____ ______
* ______ face
* Extra _____ and body hair
* Thin skin-- _______
* ______ arms and legs
* ______ Cheeks
* _________ hair
* Stretch ______
* Buffalo Hump
* Moon Face
* Face
* bruising
* thin
* red
* marks
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148
Hyperaldosteronims (Conn Syndrome) is the _______ secretion of _________ from a functional ______ that acts __________ of a physiologic stimulus.
* excessive
* tumor
* independently
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149
Hyperaldosteronims (Conns Syndrome)
* _____ > ______
* Occasionally associated with ______________, _________________ or acromegaly.
* women>men
* Pheochromocytoma
* hyperparathyroidism
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Secondary Hyperaldosteronism: presents when serum _______ is increased, stimulating the release of _____________.
* renin
* aldosterone
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What does the TRH stumulation test assess?
functional state of the TSH-secreting mechanism, and is used to test pituitary function
## Footnote
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152
Symptoms of Hyperaldosteronism (Conns Syndrome):
* _______
* _________kalemia
* hypokalemia _______ ________-
* HTN
* Hypokalemia
* Hypokalemia metabolic alkalosis
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153
Hyperaldosteronism (Conn Syndrome) is diagnosised with Spontaneous _______ in presense of systemic ______.
* hypokalemia
* HTN
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154
In Primary Hyper-Aldosteronism, plasma _____ activity is ______.
* renin
* supressed
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155
In Seconday Hyper-Aldosteronism the plasma ______ activity is ______.
* renin
* high
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Long-term ingestion of _____ can cause a syndrome that mimics the features of ______________________. Which include HTN, __________ and suppression of ______.
* licorice
* hyperaldosteronism
* hypokalemia
* RAAS
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157
Hyperaldosteronism (Conn Syndrome):
* Competetive aldosterone antagonist (________)
* _____ replacement
* antihypertensives
* diuretics
* ________ removal
* possible _______________
* Spironolactone
* Potassium
* tumor
* adrenalectomy
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158
Hypoaldosteronism is ________ in the absence of ________ insufficiency.
* hyperkalemia
* renal
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159
Hypoaldosteronism:
* Hyperkalemia may be enhanced by ________.
* _________ metabolic acidosis is common.
* hyperglycemia
* Hypercholemic
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160
Hypoaldosteronism patients may experience ____ _____ d/t hyperkalemia, ________ HoTN, and ___________
* heart block
* orthostatic
* hyponatremia
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161
Hypoaldosteronims lack of aldosterone may be caused by ________ deficiency of aldosterone synthetase or hypoeninemia d/t defects in the ________ apparatus or _______ inhibitors.
* congential
* juxtaglomerular
* ACE
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162
Hyporeninemic Hypoaldosteronism typically occus in pts > ____ years old with Chronic ________ failure or _______ _______.
* 45 years
* Renal
* Diabetes Mellitus
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__________ - induced ________ deficiency is a reversible cause of Hyporeninemic Hypoaldosteronism.
* Imadomethacin
* prostaglandin
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164
Treatment of Hypoaldosteronism includes liberal _____ intake and daily administration of ____________.
* Sodium
* fludrocortisone
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165
Name the (2) types of Adrenal Insufficency
* Primary
* Seconday
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166
Primary Adrenal Insufficency is known as ______ disease
Addisons
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167
Primary Arenal Insufficency (Addison dz) is when adrenal glands unable to produce enough ________, ___________ and adrogen hormones.
* glucocorticoid
* mineralcorticoid
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168
What is the most common cause of autoimmune adrenal destruction.
* Primary Adrenal Insufficiency (Addison)
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169
In Primary Adrenal Insufficiency (Addison) >____% of the gland must be involved before signs appear.
90%
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170
Secondary Adrenal Insufficiency: ______________ -pituitary dz or suppression leading to _______ in the production of CRH or ACTH.
* hypothalmic
* failure
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171
Seconday Adrenal Insufficency is a deficiency of ________, while Primary (Addison) Adrenal Insufficency is a deficency in glucocorticoid, mineralocorticoid and _________ hormones.
* glucocorticoid
* adrenal
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172
Seconday Adrenal Insufficency is caused by _______, such as with the use of synthetic glucocorticoids, _________ surgery or ___________.
*iatrogenic
* pituitary surgery
* radiation
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173
Seconday Adrenal Insufficency patients lack _________ and may demonstrate only mild ________ abnormalities.
* hyperpigmentation
* electrolyte
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174
Adrenal Insufficiency diagnosis is baseline cortisol <____ ug/dL and remains <____ after ACTH stimulation
* <20
* <20
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175
Adrenal Insufficeny postive test demonstrates a ______ response to _______ and indicates an _________ of the adrenal.
* poor
* ACTH
* impairment
176
Absolute Adrenal Insufficency is characterized by a ______ baseline cortisol and a ______ ACTH stimulation test.
* low
* postitive
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177
Relative Adrenal Insufficency is indicated by a ______ baseline cortisol and a _______ ACTH test.
* high
* positive
178
The treatment of Adrenal Insufficiency is _________.
Steroids.
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179
Pituitary gland is located in the ______ ______ + consists of Anterior + Posterior
The ANTERIOR pituitary secretes 6 hormones under control of the ________.
** name them
Over production of these hormones often assocaited with hyper secretion of _____ (cushing's) by anterior pituitary _________-
______ and ________ are made in hypothalamus + stored in POSTERIOR pituitary
To release these 2 hormones , stimulate the __________ in the hypothalamus that sense plasma osmolarity.
Sella Turcica
Hypothalamus
GH, ACTH, TSH, FSH, LH, Prolactin
ACTH ... adenomas
vasopressing (ADH) + oxytocin
osmoreceptors
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180
ACROMEGALY ::
is d/t excessive secretion of ____ _______ + most common cause is ________ in ANT pituitary gland
**Treatment? (2)
*Serum insulin-like growth factor 1 is ________
*What test measures plasma growth hormone ?
*Overgrowth of soft tissue makes pt susceptible to ... ?
*Overgrowth of surrounding cartilagenous structures can cause ? (3)
*______ ________ is common d/t nerve trapping by connective tissues
growth hormone ... adenoma
Tx = transphenoidal surgical excision of adenoma .. OR .. LA somatostatin analogue (if can't operate)
*elevated
*Oral glucose tolerance test -- elevated GH above 1 after 2 hrs of ingesting 75g glucose
*Upper airway obstruction
*hoarseness ... abnormal movement of vocal cords .. RLN paralysis
*Peripheral Neuropathy
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ACROMEGALY ANESTHESIA IMPLICATIONS ::
*difficult mask ventilation d/t _______________
*enlarged ________ and ______ predisposes to upper airway obstructions + interferes with _______ _____ visualizations during DL.
*increased distance bw lips + vocal cords d/t ______ ______
*Glottic opening may be narrowed d/t ______ ___ __________
*May require smaller ______ , video larygoscopy , or _____ ______ induction
*distorted facial anatomy
*tongue + epiglottis ... vocal cord
*mandible overgrowth
*vocal cord enlargement
* ETT ... awake fiberoptic
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182
SIADH ::
Treatment ? (4)
Hyponatremia treated with ____ _____ raising it less than within 24 hrs?
*fluid restriction , salt tablets ,, loop diuretics ,, vasopressin antagonists
*hypertonic saline @ <8 mEq/L within 24 hrs
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183
What can happen to the patients airway if they expereince unilateral trauma to the thryoid?
How long does it take the thyroid to return to normal?
* hoarseness but no airway obstruction
* function return in 3-6 months
## Footnote
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184
What causes permanent hoarsness for a patient after thyriod surgery?
Ligation or transection of the nerve
## Footnote
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185
How does bilateral traurma effect the patient after surgery?
* cause airway obstructin
* difficulty coughing
* may warrant tracheostomy
## Footnote
Slide 38
186
Hypoparathyriodism due to thyriod surgery is caused by?
inadvertent parathyroid damage
## Footnote
Slide 38
187
What is a sign and / or symptom of hypoparathyroidism that takes place 24-48 hours postoperativiely?
hypocalcemia
## Footnote
Slide 38
188
What complication from thyroid surgery can lead to tracheal compression?
Hemoatoma
*A trach-set should be kept at bedside during immediate postop period*
## Footnote
Slide 38
189
What are the structures found within the adrenal gland?
* cortex
* medulla
## Footnote
slide 39
190
What steroids and / or hormones are synthesizes in the cortex?
* glucocorticoids
* mineralocorticoids (aldosterone)
* androgens
## Footnote
Slide 39
191
Pertaining to Adrenal Gland function ::
Hypothalamus sends ____ to the anterior pituitary, which stimulates ____ release from the anterior pituitary
* corticotropin-releasing hormone (CRH)
* corticotropin (ACTH)
## Footnote
Slide 39
192
Corticotropin is release from the anterior pituitary to stimulate the adrenal cortex to produce, ____.
Cortisol
## Footnote
Slide 39
193
Cortisol facilitate conversion of ___ to ___ .
This takes place in what part of the adrenal gland?
* norepinephrine to epinphrine
* adrenal medulla
## Footnote
Slide 39
194
How does cortisol effects glucose in the body?
* induces hyperglycemia
* reflecting gluconeogenesis
* inhibition of glucose uptake by cells
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195
What hormones casuses sodium retention and potassium excretion?
cortisol
aldosterone
## Footnote
Slide 39
196
What is a pheochromocytoma?
a catecholamine-secreting tumor that arise from chromaffin cells of the sympathoadrenal system
| 40
197
Uncontrolled catecholamine release can lead to what disease process?
* malignant HTN
* CVA
* MI
## Footnote
slide 40
198
____% are an isolated finding
____% inherited (familial)
90%
10%
## Footnote
Slide 40
199
____% occur in the adrenal medulla,
____% in organ of Zuckerkandle,
____% neck/thorax
80%
18%
2%
## Footnote
Slide 40
200
Malignant Pheochromocytoma spread to through what body system's
venous system
lymph systems
## Footnote
Slide 40
201
What is the ratio of NE:EPI that is secrete by adrenal medulla with at patient that has Pheochromocytoma?
NE:EPI , 85:15
*inverse of normal adrenal secretion*
## Footnote
Slide 40
202
Some pheochromocytoma secrete higher levels of ____and, more rarely, ____
epi
dopamine
## Footnote
Slide 40
203
How long can a pheochromocytoma attack last?
between 1min and several hours
*maybe occasional to frequent*
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204
How does the pheochromocytoma attacks occur?
* spontaneously
* triggered by injury, stress, or meds
## Footnote
Slide 41
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What are the signs and symptoms of pheochromocytoma?
* pallor
* sweating
* palpitations
* orthostatic hypotension
* cornary vasoconstriction
* cardiomyopathy
* CHF
* EKG changes
## Footnote
Slide 41
206
What are some tests that are utilize to diagnose pheochromocytoma?
* 24h urine collection
* CT & MRI
* I-metaiodobenzylguanidine (MIBG) scintigraphy
*localize the tumor*
## Footnote
Slide 41
207
A 24 hour urine collection test for a pateint that has pheochromocytoma will be postive what to substances?
metanephrines catecholamines
## Footnote
Slide 41
208
What are some pre -op consideration to take into acconut for with patients who have a pheochromocytoma?
* α blocker to lower BP
* decrease intravascular volume
* allow sensitization of adrenergic receptors
* decrease myocardial dysfunction
## Footnote
Slide 42
209
What is the most frequently used preop Alpha blocker for phepchromocytoma?
Phenoxybenzamine
*a noncompetitive α1 antagonist with some α2-blocking properties*
## Footnote
Slide 42
210
What other medication can be use to treat pheochromocytoma?
Prazosin
doxazosin
*pure α1 blockers, shorter acting w/ less tachycardia*
## Footnote
Slide 42
211
True or false: Tachycardia after an α blockade should be treated with a BB.
True
## Footnote
Slide 42
212
True or false: Give a selective BB before α blocker b/c blocking vasodilatory β2 receptors results in unopposed α agonism, leading to vasoconstriction and hypertensive crises
False: Never give nonselective BB before α blocker b/c blocking vasodilatory β2 receptors results in unopposed α agonism, leading to vasoconstriction and hypertensive crises
## Footnote
Slide 42
213
What other class of blood pressure medication is use to control HTN for patients with pheochromocytoma?
CCBs
## Footnote
Slide 42
214
DIABETES INSIPIDUS ::
Symptoms?
Initial treatment?
Neurogenic treatment?
Nephrogenic treatment?
Anesthesia?
*polydipsia , increased serum osmo , dilute urine
*IV electrolytes
*DDAVP
*low-salt , low-protein , diuretics , NSAIDs
*monitor UOP + lytes
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DIABETES INSIPIDUS ::
reflects absence of _________
*caused by destruction of _______ _________ (neurogenic)
*caused by failure of _______ ________ to respond to ADH (nephrogenic)
* the two types are differentiate based on responses to _________
>>>> this causes urine concentration in _______ type
*vasopressin
*posterior pituitary
*renal tubules
*desmopressin
*neurogenic
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SYNDROME OF INAPPROPRIATE ADH ::
occurs in diverse pathologies like ...? (4)
elevated ADH most likely to occur following ______ ________
Sx - increased urine _____ and _______ ... in presence of _______ and decreased serum _________
Decrease in sodium can result in ______ ______ and _____
*intracranial tumors, hypothyroidism, porphyria, lung carcinoma
*major surgeries
*sodium and osmolarity ... hyponatremia ... osmolarity
*cerebral edema + seizures
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